Tag Archives: Immune Hypothesis of Benson’s Syndrome

So does this mean that folks with an immune deficiency in complement C3 have some kind of protection against Alzheimer’s?

You might have autoimmune diseases and chest infections that take forever to clear, but possibly also less of your brain disappearing with age, if research on mice is relevant to people.

Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice

http://stm.sciencemag.org/content/9/392/eaaf6295

Readers of this blog from back in 2011-2012 could have predicted this, because I pretty-much predicted this with my immune hypothesis of synaesthesia and my immune hypothesis of Benson’s syndrome (a variety of dementia). I wonder how many lives could have been saved and cases of dementia prevented if the world of science had bothered to read my blog and taken my theories seriously back then and set to work finding a therapy that reduces levels of C3? How hard could that be? It happens naturally, so how hard could it be to engineer a similar process? Instead all I got for my ideas and blogging was synaesthesia researchers plagiarizing my ideas shamelessly in a speculative paper about synaesthesia (a mere triviality in the world of neuroscience compared with the tragic and expensive problem of dementia). And all this time funding for dementia research has been counted in the hundreds of millions of dollars and has given the public virutally nothing in the way of effective therapies. How much of that research funding do I get? Not one single frickin’ red cent, because I’m not a scientist. I’m just a housewife with ideas, and a blog.

 

Interesting research on synapses and the neurobiology of forgetting supports model of dementia that appears to compete with mine

The role of GluA2-containing AMPA receptors in sustaining long-term memories and in natural forgetting has been studied by an international team of researchers. They and other researchers have speculated that this process could be involved in the development of dementia. I think they are wrong. I believe that there is a distinction between normal, adaptive forgetting and the forgetfulness of dementia that results from the destruction of the brain. I have previously in this blog outlined my original ideas about the immune system, complement, synaptic pruning and a type of dementia that goes by the names of PCa or Benson’s syndrome. My money is still on high levels of complement as the prime suspect for dementia of the rear parts of the brain. Regarding Alzheimer’s, I still favour the “Prion Hypothesis” but I also understand that obesity and diabetes 2 can damage the brain. Nevertheless, I still find this recently-published piece of research interesting because it seems to shows that forgetting isn’t just the failure of some process, it is a process in itself. I also find it interesting that real memory researchers don’t write about or make sweeping statements about memory in general, they study and write about specific types of memory.

Paddock, Catharine Brain study yields clues about ‘natural forgetting of long-term memories’ http://www.medicalnewstoday.com/articles/308549.php

Paola Virginia Migues, Lidong Liu, Georgina E. B. Archbold, Einar Ö. Einarsson, Jacinda Wong, Kyra BonasiaSeung Hyun Ko, Yu Tian Wang, and Oliver Hardt Blocking Synaptic Removal of GluA2-Containing AMPA Receptors Prevents the Natural Forgetting of Long-Term Memories. Journal of Neuroscience.  23 March 2016, 36(12):34813494; doi:10.1523/JNEUROSCI.3333-15.2016

http://www.jneurosci.org/content/36/12/3481.short?sid=e7babe8d-7f41-4f13-91ca-ae7f9a68afa0

 

Wow, this is interesting

Scientists Find Vessels That Connect Immune System And Brain. June 3, 2015 | by Stephen Luntz. IFL Science.

http://www.iflscience.com/brain/vessels-found-connect-immune-system-and-brain

Structural and functional features of central nervous system lymphatic vessels

Antoine Louveau, Igor Smirnov, Timothy J. Keyes, Jacob D. Eccles, Sherin J. Rouhani, J. David Peske, Noel C. Derecki, David Castle, James W. Mandell, Kevin S. Lee, Tajie H. Harris & Jonathan Kipnis
Nature (2015) doi:10.1038/nature14432
Received 30 October 2014 Accepted 20 March 2015 Published online 01 June 2015

http://www.nature.com/nature/journal/vaop/ncurrent/full/nature14432.html

I find this most interesting for a number of reasons. Firstly, the discovery showing that the human brain has functional lymphatic vessels connecting the brain with the immune system adds to a growing collection of evidence that the immune system plays important roles within the brain, which is an apparent partial violation of the long-held concept of the “blood-brain barrier” (as was described in a dated and inadequate chapter by Dr Karl in his 2013 pop science book Game of Knowns). In 2012 I was apparently the first person in the world, at this blog, to publish the ideas that high or low levels of the “component” immune chemicals at various points in development could be the cause of conditions of the brain such as developmental synaesthesia and Benson’s syndrome or PCA. My ideas were inspired by the very exciting research in areas such as microglia, complement, synaptic pruning and MHC1 molecules.

Another reason why this new discovery linking the central nervous system with the lymphatic and immune systems by researchers from the University of Virginia is so exciting is the fact that it is an unexpected discovery, as one might have thought that human anatomy would have already been thoroughly researched and discovered through the history of medical science to date, but then again, surprising new discoveries in human anatomy have not been unknown in recent years, with discoveries of new features in the human eye, knee and clitoris, the rediscovery last year of a major white matter tract (the vertical occipital fasciculus) at the rear of the brain that could play a central role in skills such as reading, and a new shape of neuron discovered in mouse brains. These new discoveries are exciting and also rather unsettling; exciting because it appears that important new discoveries in human neuroscience and anatomy are still possible, and unsettling because genuinely surprising new discoveries in science seem to indicate that science is not a steady accumulation of knowledge and a path of upward progress, as many believe. This may or may not be surprising to you, depending on which theory in the philosophy of science you favour. I think the discoveries of the VOF and the collection of discoveries about the roles and anatomy of the immune system in the human brain could be interpreted as evidence showing how incorrect ideas in science can become widely-accepted and widely-taught and could also have delayed the progress of new discoveries in neuroscience. How much further might we have come by now in our understanding of the human brain and mind if not for the popularity of the idea that the human brain is quarantined from the immune system? Which other influential ideas about the human brain are holding us back from a clearer understanding of the brain’s workings and diseases?

Radio show about Glenda Parkin living with dementia in suburb of Perth, Western Australia

Below are the details of a recent and very interesting radio interview on Perth public radio with Glenda and Bronte Parkin and Alzheimers WA CEO Rhonda Parker, focusing on Glenda’s experiences as a person who has a form of dementia that goes by a number of names including Benson’s syndrome, posterior cortical atrophy and PCA. This is not the first time that Glenda has shared her story with the media; she previously shared her story with Perth’s daily newspaper, the West Australian, in 2011 and she has recently been interviewed for the Community Newspaper Group.

I have unusual reasons to be grateful that Glenda has shared her story with the mass media. I happened upon her story in a copy of the West while I was enjoying coffee and one of those wonderfully greasy Sausage and Egg McMuffins in a McDonald’s restaurant in 2011, after dropping someone off to a selective school that offers students places based on high ability in the area of literacy and languages. I became intrigued by the fact that the particular type of dementia described in the article appeared to be a mirror-image of the pattern of intellectual gifts that appear to run in our family, associated with synaesthesia, a harmless, genetic, developmental and memory-enhancing condition that is caused by increased connectivity in the structure of the white matter of the brain. I wondered whether there could be an undiscovered developmental basis of Benson’s syndrome that works like the opposite of synesthesia, or could it be caused by some mature-age dysregulation of some chemical that regulates growth in the parts of the brain that seem to be hyper-developed in our family, and attacked, over-pruned or somehow damaged in Benson’s. I wrote about my ideas in this blog soon after. In 2012 my thinking on this theme took an important and exciting leap ahead when I happened across a brief article in New Scientist about research by Dr Beth Stevens on microglia, complement, synaptic pruning and elements of the immune system playing a central role in the development of the brain. I figured that one or maybe more of the complement chemicals could be the chemical that regulates growth or pruning in the parts of the brain that I had written about and attempted to identify in my 2011 blog post. I wrote a brief outline of these ideas at this blog in 2012 in an article that was archived by the Internet Archive Wayback Machine in 2012. In lat 2013 I got a big surprise when I saw my idea linking the immune system with synaesthesia as the main idea of a research paper published in a peer-reviewed neuroscience journal, and all without my permission! That’s another story….

I am sure that many people listening to this radio interview would be fascinated with or even skeptical of Glenda’s account of being able to see but not perceive letters on the cover of a book. Her eyesight is not the problem, the problem lies in the visual processing areas of her brain and because of this a lady who in her impressive career has been an author of books can no longer read text or interpret symbols. Seeing is as much done in the brain as it is done in the eye and optic nerves, and a person who has no apparent problem with their eyes can lose visual perception as the result of dementia or injury or stroke.

“Simple things can be very frustrating” – Glenda and Bronte Parkin on dementia. Mornings with Geoff Hutchison. 720 ABC Perth.
09/07/2014.
http://blogs.abc.net.au/wa/2014/07/simple-things-can-be-very-frustrating-glenda-and-bronte-parkin-on-dementia.html

Jarvis, Lucy Still making a contribution: retired educators share experience of living with dementia. Community Newspapers. 2015

Hiatt, Bethany Penrhos principal’s hardest battle.  West Australian. January 3, 2011. http://au.news.yahoo.com/thewest/a/-/mp/8588194/glenda-parkin/

Postscript March 10th 2015

The West Weekend liftout of the West Australian of February 14-15 2015 has a feature story about West Australians livng with dementia on pages 10-13. he story of Glenda and Bronte Parkin is included in that article and the content makes it clear that although Glenda Parkin has a diagnosis of Benson’s syndrome which has had a negative impact on her ability to recognize symbols, writing and objects, she can still somehow navigate her way in her neighbourhood. I find this interesting as some people who have prosopagnosia, which is an impairment in face memory, also have a similar impairment in visual memory of scenes or landscapes, and thus have serious problems with navigating their way through streets and neighbourhoods. I had thought that Benson’s syndrome, a type of dementia, and prosopagnosia, a developmental disability and also sometimes acquired from brain injury, must be in many ways similar in their manifestations, as they both feature disability in face recognition, but it appears that it is not safe to make assumptions and maybe each case of these two conditions should be considered unique. I do not recall reading about Glenda Parkin’s ability to recognize faces, so maybe I should assume it is still normal, along with her ability to recognize street-scapes and scenes.

Yeoman, William Open minds. West Weekend. p. 10-13 West Australian. February 14-15 2015.

 

Finding confirmation of my beliefs and ideas, as you do

A closely related family member of mine recently scored a perfect mark on an adult literacy test geared to normal adults (which was true to form) , and another closely related family member in mid-childhood recently explained that they perceive motor vehicles as having faces and they categorize cars, utes and 4WDs into genders, square old 4WDs being male. I can see how that makes sense, but all the same I’ve never been that much of a car personifier. Ever since I was a child I’ve personified numbers and alphabet letters in great detail, along with perceiving them as essentially associated with very specific colours, and the shapes and motions of cars often make me think of hunting animals in some deeply instinctive way, but unlike my young relative and the many Australians who decorate their own motor vehicles with oversized curly eyelashes or giant imitation testes, I don’t see motor vehicles as male or female.

On the surface most people seem pretty-much normal and average, but if you make the most superficial investigation by testing or speaking with people about their thoughts and perceptions, you might find that there is an interesting and sometimes significant range of differences in the way our minds work. Grapheme-colour synaesthesia, personifying synaesthesia and elite and precocious levels of ability in reading, spelling and general literacy are just some of the interesting things that run in my family and are also experienced by me, and I am also a super-recognizer. A super-recognizer is a person who has an elite level of ability in recognizing faces or face memory, and typically can achieve perfect or near-perfect scores on tests of face memory. I believe that this co-occurrence of synaesthesia and elite abilities in face memory and literacy are no coincidence. I believe all of these things are based on hyper-connectivity or hyper-development in the rear parts of the brain including the fusiform gyrus, and also in the right hemisphere of the brain. I believe the genetic basis of this development might be linked to genes that code for particular variations in the functioning of the immune system, possibly involving the complement chemicals, microglia and synaptic pruning. I’m fascinated by the possibility that research work that has been done in the last decade linking immunology and neuropsychology can inform us about the origins of synaesthesia and also specific gifts and deficits in memory and cognition, and maybe also inform us about some types of dementia. In 2012 at this blog I explicitly identified research on the immune system, complement, microglia and synaptic pruning done by Dr Beth Stevens as a possible explanation for the origins of developmental synaesthesia, an idea that was so good that some synaesthesia researchers made it the basis of a speculative paper that was published in a peer-reviewed journal last year (they forgot to acknowledge me as the first to publish this idea). Work done on MHC1 (part of the immune system) and the brain by Carla Shatz is another area of scientific research that I find tremendously exciting, and I believe that the general area of research on the relationships between brain structure and the immune system is of such originality and importance that it should attract one or more Nobel Prizes.

Would you like to follow these steps?

First go the the Internet Archive (Wayback Machine):  https://archive.org/

Then copy and paste the web address of this blog into the search form that you will find there, removing the beginning bit, and click on “BROWSE HISTORY”:   https://superrecognizer.wordpress.com/

The results screen that comes up will show you how many times this blog has been archived by the Internet Archive over the years.

Click on the year 2012, then click on the date June 21st 2012.

The Internet Archive will display to you their archived record of the home page of this blog as recorded on June 21st 2012. You will see a blog coloured in green and blue with stories featuring photos of some sculptures seen around Perth, but the thing that you might (or might not) find interesting is the blog post that is third down the page which was first published on June 7th 2012. This is the blog post where I briefly but clearly published my ideas suggesting causal relationships between the human immune system and synaesthesia, and low levels of some of the complement immune chemicals and synaesthesia, all related to the regulation of developmental synaptic pruning and synaptic plasticity involving the activity of microglia, and in this post I also restated my previously-published speculation that the variety of dementia known as Benson’s syndrome or posterior cortical atrophy could be regarded as the opposite of developmental synaesthesia associated with special abilities in visual perception such as super-recognition ability and exceptional reading ability, a cluster of traits that appears to run in at least one family. Got that? The point I’m trying to make is that I published this stuff in June 2012, I thought of these ideas independently and as far as I can tell no one else had previously published these ideas anywhere, including in scientific journals.

Now take a look at this paper in a neuroscience journal which was published in 2013 and was received by the journal as a draft or manuscript on July 31st 2013:  http://journal.frontiersin.org/Journal/10.3389/fnhum.2013.00563/full

Do any of the themes in the paper seem familiar? Does my blog or myself receive any credit or acknowledgement in the paper? Hmm.

Regardless of any issues related to originality or acknowledgement, the important point in all of this is that here we have some ideas about a type of dementia which could conceivably have some medical or scientific use or value. My idea of linking synaesthesia with the immune system is nice but just a step in a possibly much more important sequence of ideas. I’d like to give those ideas another airing, while also restating that I thought of them a long time ago independently and claim all due credit. I hope you don’t mind.

There’s a back-story to my theory

I can show data dating back to the year 2000 that supports my theory that low levels of complement proteins, which are a part of the human immune system, specifically C3, C4 and most likely C1q, are the biological cause of the development of inherited synaesthesia (at least in some cases). Before I had thought of the idea of a link between the immune system and synaesthesia I had, at the blog, published a theory that synaesthesia is in some way the neurological opposite of a variety of dementia named Benson’s syndrome (aka PCA, posterior cortical atrophy), based on my observations and reading. I had speculated that there could be some “magical chemical” that regulated the brain in some way and that oppositely extreme levels of this magical chemical could be the biological basis of both synaesthesia and Benson’s syndrome. Back in 2012 I read a small article in New Scientist magazine that blew my mind, because it appeared that it gave me some major clues about what that magical chemical could be. The article was about the exciting work of Dr Beth Stevens on microglial pruning in the brain and the immune system’s complement proteins. The term “pruning” was familiar to me from all of my reading about synaesthesia, which is a fun heritable brain-based phenomenon which I share with some of my first-degree relatives, along with specific gifts in literacy skills. The term “complement” in the context of the immune system, and the individual names of complement proteins were also familiar to me.

Being a super-recognizer, I’m pretty good at recognizing patterns, and I recognized that all these elements of information fitted together into an important and original multi-faceted theory. I was so excited that I published a brief outline of my theory at this blog in 2012. In 2013 I was shocked to discover that a prominent synaesthesia researcher and her co-author had published a theoretical journal paper titled “The immune hypothesis of synesthesia” which even included speculation that the “complement system” could be the element of the immune system responsible for the development of synaesthesia. I found no credit given in that paper to me or my blog. As I had published my theory first I believe I should have been fully acknowledged. I never thought that this could have been a case of two separate parties thinking of the same idea independently. I read their paper through and I looked into the educational and research background of both authors and their previous publications and found no study or writing about the immune system and no indication or explanation of why they might have suddenly had their own insight linking synaesthesia with some of the many elements of the incredibly complex immune system that only an immunologist would find interesting. 

This Easter I’d like to pose the question; can Simner and Carmichael offer data dating back to the year 2000 as the basis of their published version of “the immune hypothesis of synesthesia”? I can, and I would be willing to share my data with serious medical researchers.

A while ago I was sorting through some piles of old papers that I had stowed away years ago without sorting through them. These things happen during a busy family life. These piles had been sitting around for years, some of it photocopies of articles from New Scientist magazine that had struck me as interesting but which I hadn’t always had the time to read through properly. I was amused to find that I had stowed away an article from the March 1st 2008 issue titled “Thought control” by Bijal Trivedi. It was all about exciting research by the likes of Carla Shatz, Ben Barres, Simon John, Staffan Cullheim, Eliezer Masliah, Robert Terry and Lisa Boulanger about synapse loss in dementia and the interesting things that elements of the immune system appeared to be doing in the brain, contrary to the received wisdom that there is a thing called the blood-brain barrier that keeps the immune system out of the brain. I’m not sure whether or not I had read the article back then, but I can understand why it had sparked my interest. Back then it wasn’t enough of a spark to give me the idea of a link between the immune system and synaesthesia, because back then I hadn’t even heard of the terms “super-recognizer” or “Benson’s syndrome”, in fact the concept and the term of “super-recognizer” hadn’t yet been published. Back then I had not the slightest inkling that I had better than average ability in face recognition, so I hadn’t started thinking about whether it was more than a coincidence that I was both a synaesthete and a super, and which parts of the brain might be atypical in both. I hadn’t read the human interest story in The West about a Perth citizen who had been diagnosed with Benson’s, and felt curious about how the description of that type of dementia sounded like the opposite of skills that were superior or associated with synaesthesia in myself and kin. I must have forgotten about the content of the 2008 New Scientist article, if I had ever read it at all, because it would have been the ribbon which I could have used to wrap up my package of ideas neatly. Curiosity can be rewarded, even if it takes a couple of coins before the penny drops.

 

Thank you PubPeer

Thank you PubPeer for (after some fussing about) giving me a place on the internet that is recognized by scientists to publish my objection to some researchers publishing a highly original idea that I had thought of independently and had published at this blog over a year before their draft paper was received by their publisher. I’m certain that this is a case of plagiarism, but other people object to my use of that word, so the only place you will see the word plagiarism used in relation to that matter is here at this blog.

I have already published a very full account of my side of the story at this blog, but unfortunately this blog isn’t recognized as a part of the ecosystem of commentators attached to the world of science, the people and organizations in the league of science journalists, science magazine bloggers and internet services that are supposed to review the science literature but actually appear to be automatically-generated content. PubPeer isn’t like that; it appears to be run by people, but who they are is a mystery. I can completely understand why they wish to remain anonymous. Exposing the many ways in which peer review in science publishing is broken is a pastime that I am sure could be harmful to one’s career in science.

I believe that I can make a greater contribution to science as a blogger who has no job that is in any way connected to any university or any research institution, because I don’t have to deal with career-building and politics that goes with having that kind of career, and as a result I have more “mental bandwidth” free to devote to thinking about actual science. I am not expected to teach half-interested university students or organize conferences or write full-sized published papers or book chapters, and I’m not expected to know my proper place in the scheme of things. Very ordinary physical activities that I do in my everyday domesticated life automatically activate regions of my brain that deal with conceptual thinking and memory, and as a result I am often bombarded by novel ideas resulting from a boundless miscellany of concepts flashing onto the centre stage of my mind and colliding in a quite haphazard manner. I guarantee this kind of involuntary mental activity wouldn’t happen if I spent my days comfortably sedentary inside an airless office, staring at a wall or a dusty old painting. I’ve had jobs like that in the past, and years of study at an austere and ugly university which was also pretty much the staring at a wall lifestyle. I find it ironic that study at a university can offer an environment that has an effect on thought that must surely compare with a lobotomy.

Being a nobody to the world of science has many up-sides. I don’t feel a lot of need to consciously or unconsciously self-censor my ideas and publications to fit in with the beliefs and fashions of researcher peers (whether they make sense or not), and I don’t limit my thoughts to my job description, because I have no job description (and I also unfortunately have no salary, pay or financial benefit of any kind). Having no identity in the world of science means I also have no specialization or niche, leaving me free to see and write about a completely obvious connection between synaesthesia, an area of science typically researched by research psychologists and non-clinical neuroscience/psychiatry researchers, and the human immune system, an area of science that has I guess typically been researched by practicing medical doctors in the specialties of immunology or rheumatology. For sure there have been in the last ten years or so a group of pioneering and original researchers who have researched the incredibly complex ways in which the human immune system impacts on brain development, but I don’t think any of them have linked their work with synaesthesia or any particular type of dementia, as I have.  I’m guessing that they haven’t written about synaesthesia because they feel that it is too trivial a matter for them to bother with, which is probably a defensible point of view, as synaesthesia isn’t a disorder and I’ve never heard of a synaesthete who is looking for a cure. I feel free to write about concepts such as dementia, the complement immune chemicals and synaesthesia that are areas that are beyond my expertise, because I have no recognized area of scientific expertise or any recognized career in science. A lot of words have been written about the concept of intellectual freedom in academia, but I have found that being a non-entity outside of all that is a state that offers the most intellectual freedom. It’s a bit like being the invisible man; you can get up to all kinds of stuff but you can’t hope for recognition, because you have no face and no identity.

Being nobody is a state of freedom but it certainly has it’s frustrations, like having no income as reward for any of the work I put into this blog and the ideas published in it, and having no recognition, not even on the internet, but the most frustrating thing is the way that my most important idea has had no apparent impact in science. I’m not referring to my idea linking the immune system with synaesthesia, which was just an amusing step in my journey to the much more important idea that one particular type of dementia, known by the names Benson’s syndrome or posterior cortical atrophy or PCA, could be caused by an excess of one or more of the complement immune chemicals. Surely this is an idea that could be researched. Surely this is an idea that could lead to a number of different ideas for therapies if it turns out to have some value. Surely this is an idea worth at least checking, for if it reflects reality it surely has the potential to save minds and brains and lives. HELLO! Is anybody listening?

P.S. Late last month an Australian biotechnology company plunged on the stock market following the announcement of the failure of their drug aimed at treating Alzheimer’s dementia during a stage of a study. After years of hoopla and hype about drug companies finding a cure for Alzheimer’s or dementia, and anyone’s guess how much money spent on studies, all they can offer is symptomatic treatments. The story has been one failure after another. Benson’s syndrome is considered by some to be a variant of Alzheimer’s disease. Whether it is or not, maybe it is high time for researchers to stop obsessing about plaques in the brain and look at the immune system and the brain. My money is on C3 and C4 as concepts to focus on in a search for an understanding and cure for dementia. Would it kill you dementia researchers to accept some advice from a Perth blogger who is nobody in particular, and put my name on your research paper if my idea works out?

Some ideas that I’d like to (explicitly) lay claim to (right now) in 2014

A note of warning – If you are thinking about copying or plagiarizing any of the text, ideas or descriptions in this post or using it in your own work without giving me (C. Wright, author of the blog “Am I a Super-recognizer?”) the proper acknowledgement and citations, then think again. If you do that you will be found out and my objection will be well publicized. If you believe that you published any of these ideas before I did, please let me know the details in a comment on this article. If you want to make reference to this blog post or any of the ideas in it make sure that you state in your work exactly where you first read about these ideas. If you wish to quote any text from this post be sure to cite this post at this blog properly. There are many established citation methods. If you quote or make reference to material in this blog in your work, it would be a common courtesy to let me know about your work (I’m interested!) in a comment on any of the posts in this blog. Thank you.

The idea that Benson’s syndrome or posterior cortical atrophy or PCA, a variety of dementia, is caused or develops in a way that can be seen as the opposite of the synaesthesia linked with exceptional visual memory and literacy skills that runs in my family (this idea has been explored previously in this blog).

The idea that the above cited states develop or are caused in a way that makes them seem like opposites because they both affect the same or similar areas of the brain, but in opposite ways.

The idea that the above described process happens because Benson’s syndrome and our variety of synaesthesia are both mediated by the same or similar natural chemical or cells or biological agent in the brain, one caused by high levels of the mystery substance and the other caused by low levels (a hypothesis that I briefly suggested in January 2011).

The idea that one of the many known or unknown elements of the immune system that impact brain development is the mystery substance referred to above (a hypothesis that I briefly outlined in 2012).

The (implied in above ideas) idea of the immune hypothesis of synaesthesia. (This idea was first published by me in 2012 in a blog post archived here, was I believe plagiarized in 2013 here, and was the subject of my plagiarism claim here.)

The idea that one or more of the complement immune chemicals is the  mystery substance referred to above.

The idea that the C3 complement immune chemical  is the  mystery substance referred to above.

The idea that synaesthesia is linked with one or maybe more immune diseases or conditions caused by low levels of complement.

The idea that genes for synaesthesia stay quite common in the gene pool because of some associated cognitive advantage (probably superior memory) that balances out any disadvantages caused by deficiencies in the immune system.

The idea that some or many people unintentionally experience a memory process that operates in a similar way to the method of loci memory technique in their everyday lives, unintentionally forming long-term associations between individual learned concepts and individual visual memories of scenes (I have named this phenomenon Involuntary Method of Loci Memorization or IMLM).

The idea that IMLM operates in such a similar way to synaesthesia that one could argue that it is a type of synaesthesia.

The idea that synaesthetes are more likely to experience IMLM than non-synaesthetes.

The (implied) idea that the method of loci memory technique is similar to or a type of synaesthesia.

The idea that synaesthetes might have a natural advantage in using the method of loci because the method of loci is similar to or is a type of  synaesthesia. This idea that seems likely in light of the case of “S” the Russian memory performer with many types of synaesthesia described by Luria. 

The idea that IMLM is a phenomenon that is caused by enhanced synaptic plasticity throughout the life span.

The idea that IMLM is a phenomenon that is caused by enhanced synaptic plasticity throughout the life span and can thus be used as an indicator of which synaesthetes are synaesthetes due to enhanced synaptic plasticity throughout the life span rather than other possible causes of synaesthesia. Support for this idea comes from the fact that IMLM appears to be a non-developmental variety of synaesthesia that can form new long-term associations in adolescence and adulthood.

The idea that IMLM is a phenomenon that is caused by the unusual possession of levels of synaptic plasticity typical of a young child, during adolescence or adulthood.

The idea that IMLM is caused or enhanced by some characteristic of the immune system that affects the functioning of the brain. Many different elements of the incredibly complex immune system are thought to affect the functioning or development of the brain, and could thus be involved in IMLM, including the complement system, microglia and the MHC class I molecules. Researchers such as Beth Stevens and Carla Shatz have investigated this exciting area of neuroscience. In 2012 I hypothesized at this blog that synaesthesia could be caused by low levels of complement, this idea implying that the immune system is directly involved in synaesthesia (or at least some cases of synaesthesia). I believe these ideas were plagiarized in a paper published in 2013.

The idea that IMLM is similar to the “Proust phenomenon” in that it is very similar to synaesthesia or is a type of synaesthesia and involves episodic or autobiographical memory as a concurrent.

The idea that phonics as a foundational reading skill is similar to or is arguably a type of synaesthesia in that it involves the involuntary association of individual speech sounds with individual printed letters or combinations of letters, as the result of learning in early to mid childhood.

The idea that at least one type of dyslexia is like a deficiency of synaesthesia.

The implied idea that if synaesthesia has as it’s basis hyperconnectivity in the white matter of the brain, dyslexia as an opposite of synaesthesia or a deficiency of synaesthesia is or could be caused by hypoconnectivity in the white matter of the brain (I suspect there might be existing research evidence that supports this idea).

The implied idea that in at least one cluster or grouping of cases synaesthesia is associated with superiority in literacy or reading skill.

The idea that synaesthesia can happen in different regions of the brain, and because of this the experience of various types of synaesthesia can vary in detectable ways because of the influence on the synaesthesia of the varied ways that different areas of the brain operate. This can mean that one synaesthete can experience different types of synaesthesia that operate in very different ways, for example, some types of synaesthesia more rare or spontaneous or intrusive than other types. (I am not completely sure of the originality or the novelty of all of this idea.)

The idea that there is an association between synaesthesia and super-recognition that is not merely coincidental.

The idea that synaesthesia is a type of memory or learning. (Not sure if I’m the first to note this obvious fact).

The idea that synaesthesia concurrents are re-experienced memories, or re-activated “learnings” of concepts, not perceptions. (Not sure if I’m the first to note this obvious fact). In support of this idea I can assert that synaesthesia is like face recognition in that both are visual memory-based phenomena which are subject to the Verbal Overshadowing Effect or something very similar. My assertion that synaesthesia is subject to the verbal overshadowing effect is based on my own observations (outlined elsewhere in this post).

The idea that super-recognizers should or could be trained and employed as expert consultants in the practice of medical genetics.

The idea that medical geneticists and all types of medical specialists need to have a super-recognizer level of face memory or face recognition ability, so that they can intuitively and quickly recognize medical facies.

The idea that there is no clear point of distinction between medical facies or faces associated with genetic syndromes and normal faces.

The idea that super-recognizers could be used to facially identify blood relatives of a person or persons.

The idea that super-recognizers could be used to facially identify the specific ethnicity of a person.

(below ideas added January 28th 2014)

The idea that super-recognition or being a super-recognizer could develop as the result of an unusual level of fascination with the visual appearance of landscapes or scenes, rather than from a fascination with faces, and thus be a side-effect hyper-development of a part of the brain that serves two similar functions.

The idea that super-recognition or being a super-recognizer could, at least  in some cases, develop as the result of a general hyper-development of the visual sense to compensate for problems in the auditory sense during childhood such as temporary deafness, recurrent ear infections, glue ear or poor auditory processing.

(below idea added February 1st 2014)

The idea that lexical-gustatory synaesthesia is an exaggerated form of some kind of evolutionary adaptation in the brain that biologically primes the mind to attend to or react to speech on the subject of food (this idea was discussed at this blog in a post dated January 27th 2011, with more consideration in a later post).

(below ideas added February 6th 2014)

The idea that creativity might be immediately enhanced during and only during the duration of physical or visual-spatial activity because the activity activates areas of the brain associated with movement and in turn these areas activate other areas of the brain including those that give rise to conceptual thinking, and the increased activation makes novel associations between diverse thoughts and concepts more likely, and that this process is like synaesthesia or is a type of synaesthesia, and the types of physical activity that are the most effective inducers of this effect might be highly specific, highly specific in effects, highly varied between individuals and highly idiosyncratic, as is typical of synaesthesia inducers and concurrents. Driving a car can act as an inducer of this effect. (I have gone some way to exploring this idea in past posts.)

The idea that mental flexibility might be immediately enhanced by the above effect, which I will name “movement – thought-flexibility synaesthesia”.

The idea that thinking might be immediately enhanced by the above effect.

The idea that memory might be immediately enhanced by the above effect.

The idea that the above effect is similar to embodied cognition or is a type of embodied cognition.

(below ideas added February 14th  and  February 20th 2014)

The idea that synaesthesia is like the process of face recognition (and vice versa), because they both

– are subject to the verbal overshadowing effect or something similar

– are automatic

– are involuntary

– have a sensory inducer, in face recognition always visual, in synaesthesia I think most frequently visual

– have or can have a concurrent that could be described as a memory, a concept or a personality (I’m comparing face recognition with personification synaesthesias and the synaesthesias that I have described at this blog which have visual memories of scenes as concurrents)

– are or can be visual in both the inducer and concurrent

– typically involve the fusiform gyrus

– involve set pairings of inducers and concurrents (same person’s face seen before then recognized later)

– involve set parings of highly specific inducers and concurrents (I recognize that an employee at my local supermarket has a sister who has just started working there too, as their faces and bodies and hair are near-identical, but for the extra acne and the more receding chin of the new employee. They are very similar in appearance but my discrimination is highly specific, just as I can recognize that the green wall on the lower floor of a public library is close to but not quite the same colour as Tuesday.)

– both can have, but do not always have an actual face as an inducer (we can recognize the faces of celebrities in photos, caricatures and art, even seeing Marilyn Monroe’s face in a pattern of brown coffee cups stuck to the wall at the coffee shop at the art gallery.)

(below idea added February 17th 2014)

“My particular interest in personification is my own theory that personification synaesthesia (as experienced by myself) or something like it gives rise to superiority in face memory (or being a super-recognizer) by naturally making the faces of unknown people more memorable and interesting”

The above is a quote from an article that was published at the blog in October 2013.

(below ideas added February 19th 2014)

The idea that the synaesthesia brain is the result of the developmental influence or shaping from, or the adaptation to, the behavioural phenomenon of “flow” as described by Mihaly Csikszentmihalyi.

The idea that synaesthesia, intellectual giftedness or high IQ and autism or Asperger syndrome seem to coincide more often than chance because gifted and autistic kids are more likely to experience “flow” and this in turn can influence the developing brain in a way that gives rise to synaesthesia.

(below ideas added February 20th 2014)

The idea that the genuine conscious awareness of synaesthesia is a threshold phenomenon that operates in conflict or competition with conscious thinking, meaning that consciously thinking about synaesthesia can inferfere with the perception of concurrents, and synaesthesia must reach a particular level of intensity before it interrupts the experience of consciousness and becomes itself the subject of conscious awareness. I think that the idea that thinking about synaesthesia can interfere with the perception of synaesthesia might be related to the “verbal overshadowing” effect which has been described and debated about by researchers. In fairness I should point out that Mark C. Price speculated in the recently published (2013) Oxford Handbook of Synesthesia that synaesthesia could be subject to the verbal overshadowing effect. My own ideas were arrived upon independently from Price’s writing or work.  I base the ideas of synaesthesia being a threshold phenomenon which can also be interfered with by conscious thinking on a number of my own observations. In direct contradiction to what I had expected to find, my scores for accuracy for individual letters and numbers in The Synesthesia Battery (a scientifically-validated online test of synaesthesia) were lower for the numbers and letters that have colours that I find beautiful and which I have thought about to some degree, while my best accuracy was for the numbers and letters that have the dull and ugly colours. It seems the less I think about the concurrents the more accurately I can percieve them when they are evoked. I have also noticed that most of the types of synaesthesia that I experience I was not consciously aware of before I started to think about and examine the idea of synaesthesia. I never realised that I had complete stability in the colours I associate with months and days of the week till I tested myself. While I had a dim awareness of colour colouring my thoughts, I’d not realised that this worked like synaesthesia till I went looking for a pattern using simple testing. My fine motor movement-visual memories of scenes synaesthesia evokes concurrents that are so fleetingly and subtly experienced that they just feel like random thoughts, and indeed I now believe it is possible that the random thoughts of many or even all people are in fact synaesthesia of various types. I have also observed that there are some very unsubtle and intrusive types of syn that I experience, and they are typically rarely experienced and are associated with people, emotions, faces, singing voices or music that I find striking or novel as inducers. Because of the circumstances of these examples of synaesthesia, I think some kind of threshold is being breached when these types of synaesthesia are experienced by me.

The idea that one of the established defining criteria for synaesthesia, that it gives rise to perceptions or concurrents which are “consistent and generic (i.e., simple rather than pictorial)”, is wrong, and specific categories of memories of complex visual images such as faces and scenes, which are processed in the fusiform gyrus, can also be experienced as genuine synaesthesia concurrents. I base this assertion on the fact that I often involuntarily experience synesthesia concurrents of this type, and I have written about such experiences right from the first post in this blog which was published in 2010. I have also named types of synesthesia that have complex visual memories as concurrents: the strange phenomenon, fine motor task – visual place memory synaesthesia, involuntary method of loci memorization, etc. There are also many accounts or scientific observations of synaesthesia with complex visual concurrents in the scientific literature on synaesthesia.